From the Division of Cardiology, Peking University First Hospital, Beijing (J.L., S.L., T.Y., Y.H.).
Key Laboratory of Molecular Cardiovascular Sciences of Ministry of Education, Health Science Center (J.L., C.Z., H.X., S.L., T.Y., B.F., M.Z., X.W., Q.Z., S.L., Y.Z., R.W., X.S., T.W., J.G., B.P., Y.H., L.Z., W.H.), Peking University, Beijing.
Arterioscler Thromb Vasc Biol. 2019 Mar;39(3):513-522. doi: 10.1161/ATVBAHA.118.311749.
Objective- We aimed to assess whether exposure to higher levels of ambient air pollution impairs HDL (high-density lipoprotein) function and to elucidate the underlying biological mechanisms potentially involved. Approach and Results- In the Beijing AIRCHD study (Air Pollution and Cardiovascular Dysfunction in Healthy Adults), 73 healthy adults (23.3±5.4 years) were followed-up with 4 repeated study visits in 2014 to 2016. During each visit, ambient air pollution concentrations, HDL function metrics, and parameters of inflammation and oxidative stress were measured. Average daily concentrations of ambient particulate matter in diameter <2.5 μm were 62.9 µg/m (8.1-331.0 µg/m). We observed significant decreases in HDL cholesterol efflux capacity of 2.3% (95% CI, -4.3 to -0.3) to 5.0% (95% CI, -7.6 to -2.4) associated with interquartile range increases in moving average concentrations of particulate matter in diameter <2.5 μm and traffic-related air pollutants (black carbon, nitrogen dioxide, and carbon monoxide) during the 1 to 7 days before each participant's clinic visit. Higher ambient air pollutant levels were also associated with significant reductions in circulating HDL cholesterol and apoA-I (apolipoprotein A-I), as well as elevations in HDL oxidation index, oxidized LDL (low-density lipoprotein), malondialdehyde, and high-sensitivity C-reactive protein. Conclusions- Higher ambient air pollution concentrations were associated with impairments in HDL functionality, potentially because of systemic inflammation and oxidative stress. These novel findings further our understanding of the mechanisms whereby air pollutants promote cardiometabolic disorders.
目的- 我们旨在评估暴露于更高水平的环境空气污染是否会损害高密度脂蛋白(HDL)功能,并阐明潜在涉及的潜在生物学机制。
方法和结果- 在北京市 AIRCHD 研究(空气污染与健康成年人心血管功能障碍)中,73 名健康成年人(23.3±5.4 岁)于 2014 年至 2016 年期间进行了 4 次重复的研究随访。在每次访问中,均测量了环境空气污染浓度、HDL 功能指标以及炎症和氧化应激参数。环境中直径<2.5μm 的颗粒物的平均日浓度为 62.9μg/m(8.1-331.0μg/m)。我们观察到 HDL 胆固醇流出能力显著下降 2.3%(95%置信区间,-4.3 至-0.3)至 5.0%(95%置信区间,-7.6 至-2.4),这与参与者就诊前 1 至 7 天内直径<2.5μm 的移动平均颗粒物浓度和交通相关空气污染物(黑碳、二氧化氮和一氧化碳)的四分位间距增加有关。较高的环境空气污染物水平也与循环 HDL 胆固醇和载脂蛋白 A-I(载脂蛋白 A-I)的显著降低以及 HDL 氧化指数、氧化型 LDL(低密度脂蛋白)、丙二醛和高敏 C 反应蛋白的升高有关。
结论- 较高的环境空气污染浓度与 HDL 功能障碍有关,这可能是由于全身炎症和氧化应激。这些新发现进一步加深了我们对空气污染物促进代谢紊乱的机制的理解。